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• W1981302308 abstract "Abstract The γc-cytokines are critical regulators of immunity and possess both overlapping and distinctive functions. However, comparative studies of their pleiotropic effects on human T cell–mediated tumor rejection are lacking. In a xenogeneic adoptive transfer model, we have compared the therapeutic potency of CD19-specific human primary T cells that constitutively express interleukin-2 (IL-2), IL-7, IL-15, or IL-21. We demonstrate that each cytokine enhanced the eradication of systemic CD19+ B-cell malignancies in nonobese diabetic/severe combined immunodeficient (NOD/SCID)/γcnull mice with markedly different efficacies and through singularly distinct mechanisms. IL-7– and IL-21–transduced T cells were most efficacious in vivo, although their effector functions were not as enhanced as IL-2– and IL-15–transduced T cells. IL-7 best sustained in vitro T-cell accumulation in response to repeated antigenic stimulation, but did not promote long-term T-cell persistence in vivo. Both IL-15 and IL-21 overexpression supported long-term T-cell persistence in treated mice, however, the memory T cells found 100 days after adoptive transfer were phenotypically dissimilar, resembling central memory and effector memory T cells, respectively. These results support the use of γc-cytokines in cancer immunotherapy, and establish that there exists more than 1 human T-cell memory phenotype associated with long-term tumor immunity." @default.
• W1981302308 created "2016-06-24" @default.
• W1981302308 creator A5057581441 @default.
• W1981302308 creator A5059625599 @default.
• W1981302308 date "2010-04-29" @default.
• W1981302308 modified "2023-10-16" @default.
• W1981302308 title "IL-7 and IL-21 are superior to IL-2 and IL-15 in promoting human T cell–mediated rejection of systemic lymphoma in immunodeficient mice" @default.
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• W1981302308 doi "https://doi.org/10.1182/blood-2009-09-241398" @default.
• W1981302308 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2867264" @default.
• W1981302308 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20190192" @default.
• W1981302308 hasPublicationYear "2010" @default.
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